An Introduction to Plant Immunity

By Dhia Bouktila and Yosra Habachi

An Introduction to Plant Immunity is a comprehensive guide to plant immunology and stress response. The book covers the topic in 21 detailed chapters, starting from an introduction to the subject to the latest knowledge about plant disease resistance. The topics covered in the book include plant pathogens, plant diseases, plant immunity, passive defense mechanisms, acquired resistance, molecular genetics of plant immunology, protein function and genetic engineering. Each chapter provides a reader-friendly introduction along with clear sections detailing each topic. Additionally, detailed references for further reading are also provided. The combination of basic and advanced information on plant immunity make this book an essential textbook for students in botany and plant biology courses. Researchers interested in plant genomics and the effects of environmental and microbial interactions on plants will also benefit from this informative reference.

• Language: English
• Publisher: Bentham Science Publishers
• Release date: May 24, 2021
• ISBN: 9781681088020

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Introduction

Dhia Bouktila, Yosra Habachi

The survival of most organisms under various environmental conditions depends on the presence of general immune mechanisms, governed by an integrated genetic system. Plants, despite their immobility, have developed various sophisticated and effective mechanisms to recognize and combat pathogens during their attacks. Plant immunity is defined as the ability of plants to contain the damaging effect of a pathogen or pest. Plants contain the genetic information necessary to defend themselves from attack by a multitude of plant pathogens and pests such as viruses, bacteria, insects, nematodes, fungi and oomycetes. This defense can operate at different levels, using either preexisting passive defense systems (cuticle, wax, thorns, chemical compounds, etc.), or active defense systems appearing after the perception of aggression. In most cases, the first line of defense is sufficient to repel the pathogen, but sometimes the constitutive barriers are not sufficient and the second, active, line of resistance will be required.

Cell wall penetration introduces microbes to the plant plasma membrane where they will be confronted with extracellular surface receptors that detect pathogen-associated molecular patterns (PAMPs). This detection of microbes on the cells surface sets up PAMP-triggered immunity (PTI), which hopefully prevents the infection well before the pathogen begins to spread in the plant. That being said, pathogens have evolved strategies to disrupt PTI by secreting specific proteins, called effectors, in the cytosol of plant cells, which affect the efficacy of primary resistance (PTI). Once pathogens have gained the potential to eliminate primary defenses, plants, on the other hand, will establish a more advanced framework for the detection of microbes, termed effector-triggered immunity (ETI). In the scenario of ETI, the products of major resistance (R) genes, normally intracellular receptors, perceive the associated effector molecules released by the pathogen inside the host cell. Interplay between effectors and intracellular receptors activates a dynamic signaling network to gain disease resistance (McDowell and Dangl 2000). In fact, plant disease resistance conferred by R genes is usually supported by an oxidative burst, which is a rapid generation of significant amounts of reactive oxygen species (ROS). This ROS output is necessary for

another component of the resistance process, called hypersensitive response (HR), a form of programmed cell death that is assumed to restrict pathogen access to the plant.

Finally, at the molecular level, the plant coordinates the transcription of a variety of genes whose sole objective is resistance. The success of the plant depends on the intensity and speed of the perception of the pathogen signals and their transmission in it to produce an effective response against the pathogen. In Arabidopsis, the identification of pathogen-responsive genes is the subject of numerous studies. It has been found that no less than 25% of the genes identified in this model plant species have a transcriptional level affected following the attack of a pathogenic agent. In this way, a deeper knowledge of the basic processes involved in defense responses would make it easier to interpret the interactions between plants and pathogens and allow better resistance of plants, especially in species of agronomic interest.

The relationship between a plant and a harmful organism (i.e. pathogen or pest) depends on the environmental conditions, the properties of the harmful organism and the plant’s ability to defend itself. The concomitant evolution at the genetic level, including the plant and its pathogenic organism, is a coevolutionary process, which means a specific reciprocal interaction, between the plant and the pathogen. It obviously follows that a large part of the diversity of the living world comes from this coevolution between plants and pathogens, which seems to be an interminable arms race: a species induces a behavioral response to selection pressure imposed by another antagonistic species and the latter changes its behavior in response to the change in the first species. In all coevolutionary systems, the two partner species seek to stabilize with a balanced genetic structure. However, the structure of the genomes of any living organism is constantly modified according to the evolutionary race, via, both, small (point mutations) or large-scale (whole-genome duplications) events.

When a pathogen colonizes a plant, or a pest chooses it as a food resource, this will exert a selection pressure on the plant, thus reducing its fitness. The plant will react in two ways, either it definitively eliminates the aggressor; it is, in this case, a resistant plant, or it accepts the invasion by activating a compensation process; it is, in this case, a tolerant plant. Thus, in-depth knowledge of the genetic defense mechanisms involving resistance genes against biotic stress in plants is a prerequisite for the implementation of management programs and effective control, taking into account of the concomitant evolution of the two protagonists involved.

Contrary to popular belief, the first study linking the development of a disease to a microorganism was not carried out by Robert Koch on the tuberculosis Bacillus in 1890. Instead, at the beginning of the 19th century, the cause of wheat decay was identified by the Swiss Isaac-Bénédict Prévost (1755-1819). This researcher analyzed the cycle of the microscopic parasite responsible for this disease, and developed a mixture capable of eradicating it. However, this work was forgotten because of the preference, in official scientific circles, for the theory of spontaneous generation¹. In 1861, the German Anton de Bary, considered as the father of phytopathology, did the same by proving that the terrible epidemic of potato late blight responsible for the great famine of Ireland of the 19th century was caused by the filamentous pathogen Phytophtora infestans (Matta 2010). More recently, the fungus Helminthosporium oryzae was the cause of one of the most significant famines of the 20th century. In 1943, the destruction of rice crops by this fungus was responsible for the deaths of three million people in Bengal (Padmanabhan 1973). The practice of intensive farming since the late 1970s encouraged the development of epidemics. Indeed, monoculture on very large plots and the shortening of crop rotations have led to a loss of diversity in cultivated plants, which are no longer able to resist pathogenic agents on a long-term basis (Ricci et al. 2011). Control of phytopathogenic agents is, therefore, a major issue to ensure food security for populations.

To limit the damage caused by pathogens in agrosystems, humans have developed various control methods. First of all, cultural practices make it possible to limit the quantities of inoculum, by crop rotation and the burial of residues. Chemical control has also been widely used since the start of the 20th century and has significantly increased yields (Hirooka and Ishii 2013). Chemical treatments of crops effectively fight against phytophagous insects and fungal diseases. However, their possible impact on the environment is a real source of concern. In addition, as it is the case in animals and humans, chemical treatments are powerless against viral plant diseases, except in the rare cases where they attack the organisms that vector them, insects, nematodes or fungi. It is therefore necessary to develop alternative strategies to chemical control, against viruses. Finally, genetic selection is based on the use of cultivar resistance to fight against pathogens.

Two types of cultivar resistance are differentiated. Quantitative resistance is controlled by a large number of genes (polygenic resistance) associated with genome portions called Quantitative Trait Loci (QTLs) that contribute to the expression of resistance. It most often gives the plant partial resistance to a pathogen because the defenses of the plant do not completely prevent the invasion of the disease. It is therefore not blocked but only slowed down in its progression, which causes some visible damage to the plants. On the other hand, qualitative resistance is controlled by one or a few genes called R genes (mono- or oligogenic control). It most often gives the plant complete resistance to a pathogenic agent. The latter is blocked from the early stages of infection and does not cause damage. This resistance is often associated with symptoms of hypersensitivity (HR) and triggered by molecules manipulating the structure or cellular functions of the host, called effectors or virulence factors (Greenberg and Yao 2004).

In this context, the genetic dissection of quantitative resistance to diseases, a priori more durable than monogenic resistance, has progressed considerably over the past fifteen years with the development of molecular tools and genomics. However, even if numerous studies on quantitative resistance in various pathosystems have made it possible to identify QTLs of resistance, their exploitation in cultivar breeding remains difficult because of the complexity of genetic determinisms and the instability of their effects, partly due to their interactions with the genetic background.

¹ Theory stating that life may arise from nonliving matter.

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